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Induction of IgA1 and IgA2 production in immature human fetal B cells and
pre-B cells by vasoactive intestinal peptide
H Kimata and M Fujimoto
Department of Pediatrics, Faculty of Medicine, Kyoto University Hospital,
Japan.
We studied the effects of vasoactive intestinal peptide (VIP) on IgA1 and
IgA2 production in human fetal B cells and pre-B cells derived from bone
marrow. VIP induced IgA1, IgA2, and IgM production in sIgM+, CD19+ fetal B
cells stimulated with anti-CD40 monoclonal antibody (MoAb) without inducing
the production of IgG1, IgG2, IgG3, IgG4, or IgE. The anti-CD40 MoAb plus
VIP also induced IgA1, IgA2, and IgM production in sIgM-, CD19+ pre-B
cells, which was enhanced by the addition of interleukin-7 (IL-7). This
induction by VIP was specific, as the anti- CD40 MoAb plus other
neuropeptides [ie, somatostatin (SOM) or substance P (SP)] had no effect,
and moreover, the induction was specifically blocked by a VIP antagonist.
Furthermore, the anti-CD40 MoAb plus various cytokines, including IL-1
beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, transforming growth factor beta
(TGF-beta), low-molecular-weight B-cell growth factor (BCGF), and
interferon-gamma (IFN-gamma), did not induce IgA1 and IgA2 production in
fetal B cells or pre-B cells. These findings indicate that, in the presence
of costimulators, VIP may induce IgA1 and IgA2 production by isotype
switching.
Volume 85,
Issue 8,
pp. 2098-2104,
04/15/1995
Copyright © 1995 by The American Society of Hematology
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